ARRYTHMIAS AND CONDUCTION DEFECTS IN ECG LEARNING OBJECTIVES

Transcription

1 ARRYTHMIAS AND CONDUCTION DEFECTS IN ECG LEARNING OBJECTIVES At the end of the lecture, students should be able to: Name the common cardiac arrhythmias Describe the electrical events that produce them. Normal Results Heart rate: 72 to 80 beats per minute Heart rhythm: consistent and even What Abnormal Results Mean Abnormal ECG results may be a sign of Tachycardia Bradycardia Abnormal heart rhythms (arrhythmias) Cardiac muscle defect Congenital heart defect Coronary artery disease Ectopic heartbeat Enlargement of the heart Changes in the amount of electrolytes (chemicals in the blood) Past heart attack Present or impending heart attack Atrial fibrillation/flutter NORMAL ECG SINUS RHYTHM Rate - ( bpm) QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval - Normal (<5 small Squares. Anything above and this would be 1st degree block) Indicates that the electrical signal is generated by the sinus node and travelling in a normal fashion in the heart. ARRHYTHMIAS

2 Arrhythmias are abnormalities of electrical rhythm, resulting from alteration of impulse formation, impulse conduction or both. It is a disorder of the heart rate (pulse) or heart rhythm, such as beating too fast (tachycardia), too slow (bradycardia), or irregularly. PATHOLOGY OF ARRYTHMIAS Disturbances can be due to: Improper formation of impulses (ectopic beats) Delay in conduction OR Failure of conduction, o in particular in the AV node (AV BLOCK), or the bundle branches (BUNDLE BRANCH BLOCK) DISTURBANCE OF IMPULSE FORMATION Can be due to ectopic discharge (forming outside the SA node), causing depolarization of the heart muscles, causing ectopic beats. TYPES OF ARRYTHMIAS Depending upon the site of origin of ectopic beats, they can be: Escape beats (from AV node or bundle of His) Supraventricular arrythmias (from the atria) Ventricular arrythmias (from the ventricles) TYPES OF CONDUCTION DEFECTS Bradycardia - a slow heart rate <60 due to problems with the SA node's pacemaker ability, or an interruption in conduction through the natural electrical pathways of the heart. Physiological bradycardia occurs during sleep and in atheletes TACHYCARDIA Heart rate > 100 beats per minute (bpm) is known as tachycardia Supraventricular Tachycardia (SVT) - a fast heart rate >100 that originates in the (atria). The most common are: Atrial fibrillation or flutter Atrioventricular nodal reentry tachycardia (AVNRT). Ventricular tachycardia (VT) - a fast heart rate that originates in the (ventricles). Ventricular fibrillation Ventricular extrasystoles

3 Torsades de Pointes CAUSES OF ARRYTHMIAS The risk of getting a tachycardia or bradycardia varies greatly, depending on: Condition of your heart (dilated, inflammations, previous fibrous plaques) Electrolytes imbalances (K +, Na +, Ca ++ ) Endocrine abnormalities Past heart attack Some substances or drugs, including sometimes anti-arrhythmic medications. SUPRAVENTRICULAR TACHYCARDIA (SVT) A narrow complex tachycardia or atrial tachycardia which originates in the 'atria' but is not under direct control from the SA node SVTs are due to extra, abnormal electrical connections between the atria and the ventricles, the bypass tracts which allow the formation of reentrant arrhythmias P waves absent or inverted after QRS. ECG IN SVT Rhythm Regular Rate beats per minute QRS Duration - Usually normal P Wave - Often buried in preceding T wave P-R Interval - Depends on site of supraventricular pacemaker SINUS ARRYTHMIA SINUS TACHYCARDIA: This sinus tachyarrhythmia is a normal phenomenon and is due primarily to fluctuations in parasympathetic output to the heart.

4 SINUS BRADYCARDIA: During inspiration, impulses in the vagi from the stretch receptors in the lungs inhibit the cardio-inhibitory area in the medulla oblongata. The tonic vagal discharge that keeps the heart rate slow decreases, and the heart rate rises. Normal P wave, followed by normal QRS complex ECG IN SINUS TACHYCARDIA Rate - More than 100 beats per minute QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval - Normal The impulse generating the heart beats are normal, but they are occurring at a faster pace than normal. Seen during exercise ECG CHANGES IN SINUS BRADYCARDIA Rate - less than 60 beats per minute QRS Duration - Normal P Wave - Visible before each QRS complex P-R Interval - Normal Usually benign and often caused by patients on beta blockers ATRIAL TACHYCARDIA Atrial tachycardia occurs with atrial rates up to 220/min. It occurs when an atrial focus discharges regularly or there is reentrant activity producing excitation which stimulates the AV node prematurely and is conducted to the ventricles Excessive abnormally shaped P waves, may out number QRS ECG IN ATRIAL TACHYCARDIA

5 Rhythm: Regular Rate: bpm P wave: Abnormal P before each QRS (difficult to see) PR interval: < 0.20 sec QRS :< 0.12 sec ATRIAL FLUTTER Atrial rate usually greater than 300 bpm In atrial flutter, a large reentrant circuit is formed within the atrium As with SVT the abnormal tissue generating the rapid heart rate is also in the atria, however, the atrioventricular node is not involved in this case. Flutter waves, or saw tooth baseline, due to repeated P waves, and absent QRS complexes Ventricular rate greater than 150 bpm ECG IN ATRIAL FLUTTER Rate - Around 110 beats per minute QRS Duration - Usually normal P Wave - Replaced with multiple F (flutter) waves, usually at a ratio of 2:1 (2F - 1QRS) but sometimes 3:1 P Wave rate beats per minute P-R Interval - Not measurable ATRIAL FIBRILLATION A chaotic, irregular rhythm at bpm In most cases it appears to be due to multiple concurrently circulating reentrant excitation waves in both atria. However, some cases of paroxysmal atrial fibrillation seem to be produced by discharge of one or more ectopic foci. This irregular rhythm can be felt when palpating a pulse Absent P waves, irregular QRS complex The AV node responds intermittently, so ventricular rate becomes irregular, around /min

6 ECG IN ATRIAL FIBRILLATION Rhythm - Irregularly irregular Rate - usually beats per minute but slower if on medication QRS Duration - Usually normal P Wave - Not distinguishable as the atria are firing off all over P-R Interval - Not measurable Atrioventricular nodal reentry tachycardia (e.g. WOLFF-PARKINSON-WHITE SYNDROME) Refers to conduction of the electrical activation retrograde into a myocardial region, originally refractory to such currents It is an arrhythmia in which an electrical impulse is established that spins continuously between the atria and the ventricles, thus causing one form of SVT. Pathogenesis: Decreased refractory period of the myocardial tissue Enhanced automaticity Triggered activity MAY LEAD TO ATRIAL OR VENTRICULAR FIBRILLATION ECG IN AVNRT Rhythm: Regular, narrow-complex tachycardia. Rate: 150 bpm No visible P waves preceding QRS Retrograde P waves PR interval of 120ms. Ventricular tachycardia Rapid heart rhythm originating within the ventricles. VT tends to disrupt the orderly contraction of the ventricular muscle Current from ectopic foci in the ventricles (almost always from underlying disease, e.g. past M.I.plaque) Increased venticular rate on ECG

7 ECG IN VT Rhythm Regular Rate Beats per minute QRS Duration Prolonged P Wave - Not seen VENTRICULAR FIBRILLATION Rapid, chaotic ventricular arrhythmia that immediately brings to a halt all meaningful ventricular contractions ALWAYS A DEFINABLE UNDERLYING DISEASE PRESENT (except in long QT syndrome, which is hereditary) Reentry currents Electrolyte imbalance Hormonal disruption, causing sympathetic discharge(thyrotoxicosis) No definable wave appreciable. ECG IN VF Rhythm - Irregular Rate disorganized QRS Duration Not recognisable P Wave - Not seen This patient needs to be defibrillated!! QUICKLY TREATMENT OF VF: VF is a life threatening condition, as due to rapid discharge the ventricles beat so rapidly that very little or no blood at all is pumped because there is not enough time between contractions for the ventricles to fill. When VF occurs, a well-placed electrical shock across the chest may be life saving. The shock, known as defibrillation, neutralizes all the abnormal electric circuits, thus giving the heart's pacemaker a chance to kick in at a normal rate. Because the brain and heart cannot survive total loss of blood flow lasting much more than about 5 minutes, it is crucial that the shock be delivered within this time frame. A device called an AED (automatic external defibrillator) is an easy to use device, which should be made publicly available in ambulances, at offices, market places etc to deal with this life threatening emergency VENTRICULAR EXTRASYSTOLES DEFINTION:

8 Premature ventricular contractions, without atrial depolarization Ectopic foci, e.g, old ischemic infarcts, in ventricles cause these extra currents Inverted QRS complex, misshapen QRS and T and absence of a P wave preceding this contraction TORSADES DE POINTES Ventricular tachycardia with varying axis Due to antiarrythmics, creating abnormalities in electrolytes, or causing ectopic foci Increased QT interval Varying axis DELAY IN CONDUCTION Electrical problems within the heart may disrupt the heart's natural pacemaker (SA node) Sometimes a body's natural pacemaker malfunctions despite an otherwise perfectly healthy heart Lack of oxygen supply to the SA node may also cause it to malfunction In case of such disruption, the other conducting pathways of the heart, which also show automaticity, maintain the cardiac rhythm, but at a slower rate. Different intrinsic rhythm of rhythmic cells Purkinje fiber /min Atrioventricular node /min CONDUCTION DEFECTS Lead to: Sick sinus syndrome First degree heart block Second degree heart block Stokes Adam syndrome Third degree or complete heart block

9 Cardiac arrest SICK SINUS SYNDROME Disease processes affecting the sinus node lead to marked bradycardia accompanied by dizziness and syncope (sick sinus syndrome). HEART BLOCK Incomplete heart block: When conduction between the atria and ventricles is slowed but not completely interrupted. Can be: First-degree heart block: All the atrial impulses reach the ventricles but are delayed. ECG: PR interval is abnormally long. Normal in atheletes 2. Second-degree heart block: Not all atrial impulses are conducted to the ventricles. ECG: A ventricular beat may follow every second or every third atrial beat (2:1 block, 3:1 block, etc). FIRST DEGREE HEART BLOCK Rhythm Regular Rate - Normal QRS Duration - Normal P Wave - Ratio 1:1 P Wave rate Normal P-R Interval - Prolonged (>5 small squares) TYPES OF SECOND DEGREE HEART BLOCK MOBITZ TYPE I or Wenckebach phenomenon: A form of incomplete heart block, in which there are repeated sequences of beats in which the PR interval lengthens progressively until a ventricular beat is dropped PATHOPHYSIOLOGY: Conduction block of some, but not all atrial beats getting through to the ventricles through AV node(70%), or His Purkinjee system(30%). ECG: The PR interval of the cardiac cycle that follows each dropped beat is usually normal or only slightly prolonged ECG IN MOBITZ TYPE I

10 ly irregular Rate - Normal or Slow QRS Duration - Normal P Wave - Ratio 1:1 for 2,3 or 4 cycles then 1:0. P Wave rate - Normal but faster than QRS rate P-R Interval - Progressive lengthening of P-R interval until a QRS complex is dropped MOBITZ TYPE II: The Mobitz II second-degree AV block is characterized by an unexpected nonconducted atrial impulse. Pathophysiology: The conduction delay occurs infranodally. Electrical conduction usually has a constant P-R interval, in the case of type 2 block atrial contractions are not regularly followed by ventricular contraction ECG: The QRS complex is likely to be wide. The PR and R-R intervals between conducted beats are constant. ECG IN MOBITZ TYPE II Rate - Normal or Slow QRS Duration - Prolonged P Wave - Ratio 2:1, 3:1 P Wave rate - Normal but faster than QRS rate P-R Interval - Normal or prolonged but constant RIGHT OR LEFT BUNDLE BRANCH BLOCK One branch or both of the bundle of His are interrupted Abnormal conduction through the bundle branches will cause a depolarization delay through the ventricular muscle This delay shows as a widening of the QRS complex Excitation passes normally down the bundle on the intact side and then sweeps back through the muscle to activate the ventricle on the blocked side. ECG: Ventricular rate normal QRS complexes prolonged and deformed ECG IN BUNDLE BRANCH BLOCK

11 Rate - Normal QRS Duration - Prolonged P Wave Ratio 1:1 P Wave rate - Normal and same as QRS rate P-R Interval - Normal STOKES ADAM SYNDROME/ CARDIOVASCULAR SYNCOPE Refers to a sudden, transient episode of syncope, occasionally featuring seizures Second or third degree heart block, can cause inadequate blood flow to the brain and result in fainting and/or seizures. ECG changes Venticular asystole or VF COMPLETE HEART BLOCK/ THIRD DEGREE HEART BLOCK A disorder of the cardiac conduction system where there is no conduction through the AV node. Therefore, complete dissociation of the atrial and ventricular activity exists. PATHOPHYSIOLOGY: 3rd degree block or complete heart block occurs when atrial contractions are 'normal' but no electrical conduction is conveyed to the ventricles. The ventricles then generate their own signal through an 'escape mechanism' from a focus somewhere within the ventricle. The ventricular escape beats are usually 'slow'. ECG: QRS complexes being conducted at their own rate and totally independent of the P waves. ECG IN 3rd DEGREE HEART BLOCK Rate - Slow QRS Duration - Prolonged P Wave - Unrelated P Wave rate - Normal but faster than QRS rate P-R Interval - Variation Complete AV block. No atrial impulses pass through the atrioventricular node and the ventricles generate their own rhythm

12 CARDIAC ARREST Cardiac arrest is the cessation of normal circulation of the blood due to failure of the heart to contract effectively and if this is unexpected can be termed a sudden cardiac arrest or SCA. IT IS THE MOST COMMON CAUSE OF DEATH WORLD WODE PATHOPHYSIOLOGY: Ventricular fibrillation or pulseless venticular tachycardia. (both reversible by defibrillation) Or Pulseless electrical activity or asystole (no effect of defibrillation) Reflect the above SELF ASSESSMENT Name the types of arrythmias What is/ are the general underlying mechanism that cause arrhythmias? What is a conduction defect? Differentiate between Mobitz type I and Type II second degree heart block REFERENCES GUYTON AND HALL S text book of physiology GANONG S review of physiology THANKS